Garbage Disposal Drug to Slow Alzheimer’s Effects

by Daniel Calder, WebPsychology

We may be a long way off from curing Alzheimer’s disease. However, scientists may have recently discovered a drug which effectively slows the progression of the insidious disease. Rather than directly repairing damage done to the brain, however, this drug improves what neurologists are referring to as the brain’s “garbage disposal system,” whose purpose is to decrease amounts of toxic proteins associated with neurodegenerative disorders.

Taking Out The Trash

According to research conducted on mouse cognition by neuroscientists at Columbia University Medical Center (CUMC) and New York State Psychiatric Institute (NYSPI), the drug, rolipram, effectively eliminates the toxic Tau proteins associated with neurodegenerative diseases such as Alzheimer’s disease. “We have identified a new way to activate the brain’s garbage disposal system, and have shown that we can effectively use a drug to activate this system and slow down disease in a mouse model,” said research leader Karen E. Duff, PhD, professor of pathology and cell biology. While the use of rolipram itself in humans is not advisable due to the nausea that it causes, similar drugs share rolipram’s therapeutic effects on the brain without this side effect. How The Drug Affects The Brain

Brain cells must habitually clear out damaged or worn proteins. This task is performed by a tiny molecular cylinder known as the proteasome, a kind of garbage disposal system whose purpose is to grind up old proteins, recycling them into new ones. Since neurodegenerative diseases such as Parkinson’s, Huntington’s and Alzheimer’s disease entail the accumulation of these proteins in the brain’s neurons, neuroscientists believe that the function of proteasomes are impaired.

Details Of The Experiment

Researchers found that the brain of a genetically engineered mouse malfunctions in failing to prevent the accumulation of tau when these proteins stick to the proteasome and hinders its protein disposal process. According to Natura Myeku, PhD, an associate research scientist in the pathology and cell biology department at CUMC, “Something profoundly bad happens to proteasomes in diseases where abnormal proteins accumulate.” He added that his work on tau “showed that even when proteasomes are removed from the diseased brains they remain defective and can’t chew up proteins compared with proteasome from normal brains.” The administration or rolipram, however, reactivated the proteasome, successfully restoring its protein disposal process.